Heart Failure with Preserved Ejection Fraction: Hemodynamic Profile
Heart failure with preserved ejection fraction (HFpEF) and diastolic dysfunction is characterized by normal LV end-diastolic volume, normal end-systolic volume, and elevated end-diastolic pressure (Option A). This is the fundamental hemodynamic signature that distinguishes HFpEF from other forms of heart failure.
Core Hemodynamic Features
The defining hemodynamic profile of HFpEF includes 1:
- Preserved LVEF ≥45-50% (normal systolic function)
- Normal or near-normal LV chamber volumes (both end-diastolic and end-systolic)
- Elevated LV filling pressures (increased end-diastolic pressure)
- Evidence of diastolic dysfunction on echocardiography
This contrasts sharply with heart failure with reduced ejection fraction (HFrEF), where LV dilation with increased end-diastolic volumes is the hallmark. In HFpEF, the ventricle maintains normal size but becomes stiff and non-compliant, leading to elevated pressures despite normal volumes 2, 1.
Why the Other Options Are Incorrect
Options C and D are wrong because they describe elevated LV end-diastolic volume, which indicates ventricular dilation—the pathophysiology of HFrEF, not HFpEF. When the ventricle dilates, ejection fraction falls because stroke volume cannot keep pace with the enlarged chamber size 1.
Option B is incorrect because it describes normal end-diastolic pressure. The entire clinical syndrome of HFpEF depends on elevated filling pressures causing pulmonary congestion and dyspnea. Normal filling pressures would not produce heart failure symptoms 1.
Diagnostic Confirmation
The diagnosis requires three components 1:
- Clinical signs/symptoms of heart failure (dyspnea, fatigue, edema)
- Preserved LVEF ≥45-50% on echocardiography
- Evidence of diastolic dysfunction, demonstrated by:
Key Pathophysiologic Insight
The preserved ejection fraction in HFpEF is somewhat misleading. EF is maintained because both the numerator (stroke volume) and denominator (end-diastolic volume) remain normal or only mildly reduced 1. The problem is not contractility but rather impaired relaxation and increased chamber stiffness, which prevents adequate filling at normal pressures. To achieve adequate filling, pressures must rise—this is what causes symptoms 2.
Common Diagnostic Pitfall
Do not confuse preserved EF with normal cardiac function. Many clinicians mistakenly assume that normal EF means the heart is working well. In HFpEF, the heart has significant functional impairment despite normal EF. The elevated filling pressures cause backward transmission to the pulmonary circulation, resulting in dyspnea and exercise intolerance 4, 5. The E/e' ratio is the most validated single parameter for estimating these elevated pressures non-invasively, though it has only modest correlation (r=0.56) with invasive measurements 3.